荨麻疹的非IgE介导机制

Non-IgE-mediated pathogenesis of urticaria

荨麻疹是皮肤科常见疾病,以皮肤风团伴瘙痒为主要特征.长期以来,一直认为荨麻疹是肥大细胞表面高亲和力的IgE受体与抗原发生交联,引发肥大细胞脱颗粒释放组胺所致.然而,研究发现,Ⅱ～Ⅳ型变态反应及非免疫机制均可介导肥大细胞或嗜碱性粒细胞活化.肥大细胞或嗜碱性粒细胞活化后脱颗粒,释放组胺及炎症介质,共同参与荨麻疹的发生发展.正确认识荨麻疹发病的非IgE介导机制,有助于更深刻地理解荨麻疹临床表现的多样性,指导临床开展规范的过敏原检测,为治疗提供新的理念.

Urticaria is a common skin disease mainly characterized by wheals and itching.It has been long considered that the cross-linking of high-affinity immunoglobulin E （IgE） receptors on mast cells with antigens induces mast cells to degranulate and release histamines,which finally result in the occurrence of urticaria.However,recent studies have found that type Ⅱ-Ⅳ allergy and non-immune mechanisms can mediate the activation of mast cells and basophils.Activated mast cells and basophils degranulate and release histamines as well as inflammatory mediators,which are concomitantly involved in the occurrence and development of urticaria.Correct understanding of IgE-independent mechanisms in the pathogenesis of urticaria is helpful to further understand the diversity of its clinical manifestations,standardize detection of allergens in clinical practice,and to provide new theoretical basis for its treatment.